In modern medical science, it is deemed that the formation of thrombus has a certain relationship with the exorbitant platelet aggregation rate.
Thrombus originates from the local coagulation mechanism, which is covered by proliferative endotheliocyte after hyper-thrombosis of endarterium surface, while lipides and other active substances, which are released by the lysis of platelet and leukocyte, enter the mural thrombus of artery to form the atheromatous plaque gradually. Subsequent researchers find out that the disease originates from the injury in arterial tunica intima, then platelet activating factor (PAF) increases and platelets adhere and aggregate here, subsequently microthrombus is formed by fibrin deposition. Some active substances are released by the platelet after their aggregation, wherein the thromboxane A2 (TXA2) can offset the effect of platelet depolymerization and vasodilatation produced by the prostacycline (PGI2) that is synthesized by blood vessel wall and thus promotes further platelet aggregation and vasoconstriction, the platelet derived growth factor can stimulate the proliferation and contraction of smooth muscle cells and make them move towards tunica intima, 5-serotonin and fibroblast growth factor can stimulate fibroblast smooth muscle cells and endotheliocyte to produce epinephrine and ADP (adenosine diphosphate) and thus promote further platelet aggregation, Factor VIII causes the further adhesion of platelet, platelet factor 4 can make the blood vessels constrict, PAI (plasminogen activator inhibitor) inhibits the thrombolysis of thrombus. These substances aggravate the injury of endotheliocyte, which subsequently causes the following results that are all in favor of the formation of scleratheroma: LDL (low-density lipoprotein) enters tunica intima and even beneath it, monocytes aggregate in tunica intima and develop into foam cells, smooth muscle cells proliferate and move into tunica intima to phagocytose the lipids, and endothelial cells proliferate.
There are coagulation system and anticoagulation system in human blood. Under normal circumstances, these two systems keep a dynamic balance to ensure the normal flow of blood in blood vessels, which means thrombus wouldn't be formed. Under special circumstances, e.g. blood vessels have injury such as vascular sclerosis and hemadostenosis, cold weather, excessive sweating, hypotension, insufficient water drinking, etc., blood flows slowly and becomes concentrated and viscous, leading to hypercoagulation or impaired anticoagulation, and subsequently the abovementioned balance is disrupted which results in a “thrombophilic state”. Thromboembolic diseases may occur everywhere of blood vessels, wherein thrombus flows in blood vessels along with blood. If thrombus stays in cerebral artery vessels and hinders the normal blood flow of the cerebral artery, it is referred to as cerebral thrombus which thereby causes ischemic stroke attacks, and if it blocks coronary artery vessels of the heart, it causes myocardial infarction, as well as arterial thrombosis in lower extremity, deep venous thrombosis in lower extremity and pulmonary embolism, etc.
When it onsets, most thrombosis will cause severe symptoms, such as hemiplegia and aphasia for cerebral infarction, intense angina in precordial region for myocardial infarction, severe chest pain, dyspnoea, hemoptysis and other symptoms caused by pulmonary infarction, pain in legs or coldness and intermittent claudication, etc. in case of thrombosis in lower extremity. Extremely severe heart infarction, cerebral infarction and pulmonary infarction can even result in sudden death. Whereas thrombosis may have no obvious symptoms sometimes, taking the commonly observed deep venous thrombosis in lower extremity for example, patients suffering this disease just feel sour and swollen legs, and most of them often consider it as the result of fatigue or cold, and subsequently miss the optimal treatment timing. It is particularly unfortunate that many doctors often misdiagnose it as other diseases. When typical edema of lower extremity develops, the treatment of the disease will be difficult and sequela will be left. The formation of thrombus will often result in the aforesaid severe consequences, but up to now there hasn't been a drug with high efficacy without toxic-and-side effects for use in treating or preventing thrombosis.
Atractylenolide compounds, e.g. atractylenolide II, atractylenolide III, etc., derive from extracts of dried roots of compositae plant Atractylodes macrocephala Koidz. In researches of prior art, atractylenolide compounds have anti-inflammatory and antitumor effects together with properties of regulating gastrointestinal peristalsis and promoting the absorption of nutrients. Nonetheless, up to now, the effect of inhibiting platelet aggregation of atractylenolide compounds has not been reported yet.